Foretelling Preeclampsia

Preeclampsia is a leading cause of maternal death and often occurs without warning. The condition results in high blood pressure and protein in the urine. Preeclampsia may begin with mild symptoms, then progress to severe preeclampsia and to eclampsia - dangerously high blood pressure and convulsions - which may result in disability or death.

In the current study, the researchers the National Institutes of Health and Beth Israel Deaconess Medical Center present strong evidence that an imbalance of two proteins produced by the placenta is responsible for the symptoms of preeclampsia. Abnormally high levels of these proteins appear to deprive the blood vessels of substances needed to keep the lining of the blood vessels healthy. Deprived of these essential substances, the cells lining the blood vessels begin to sicken and die. As a result, the blood pressure increases, and the blood vessels leach protein into the tissues and urine.

The first of these two proteins is known as soluble endoglin. It begins accumulating in the blood of pregnant women 2 to 3 months before they develop preeclampsia. In women who developed preterm preeclampsia, levels of soluble endoglin began to rise in the 17th to the 20th week of pregnancy. In women who developed preeclampsia at full term, soluble endoglin levels rose at the 25th to the 28th week of pregnancy. Similarly, soluble endoglin levels also rose in the 33rd through the 36th week of pregnancy for women who later developed gestational hypertension.

The second protein involved in the chemical imbalance is called soluble fms-like tyrosine kinase 1 (sFlt1). The women in the study who had developed preeclampsia had increased levels of sFlt1. The increase in sFlt1 was accompanied by reduced levels of a substance, placental growth factor (PlGF). Both women with term preeclampsia and women with gestational hypertension had a simultaneous rise in soluble endoglin, and an increase in the ratio of sFlt1 to PlGF (high levels of sFlt1 and low levels of PlGF.)